Similar Datasets
Project description:Gammaherpesviruses (GHV) are DNA tumor viruses that establish lifelong latent infections in lymphocytes. For viruses such as Epstein-Barr virus (EBV) and murine gammaherpesvirus 68 (MHV68), this is accomplished through a viral gene-expression program that promotes cellular proliferation and differentiation, especially of germinal center (GC) B cells. Intrinsic host mechanisms to control virus-driven cellular expansion are incompletely defined. Using a small-animal model of GHV pathogenesis, we identify the B cell-specific latency gene M2, an MHV68 mediator of GC B cell differentiation, as a viral gene product that is sufficient to induce p53 in a manner that is dependent on Src kinase activity. To understand the function of M2 in germinal center B cells in vivo, we infected AID-cre tdTomato reporter mice with WT or M2.Stop 73.Bla MHV68. At 16 dpi, draining lymph nodes were harvested and treated with CCF4-AM. AID+ and AID+Bla+ lymphocytes were sorted from WT and M2.Stop MHV68 infected tissue and sent for ultra-low input RNA-seq analysis.
2024-12-20 | GSE285085 | GEO
Project description:Previous studies identified a role for latent herpesvirus infection in cross-protection to infection and exacerbation of chronic inflammatory diseases. Here, we compared the gene expression signature from livers, spleens and brains of mice infected with wild-type gammaherpesvirus 68 (MHV68), a mutant virus defective in the establishment of latency (ORF73.stop) or mockulum. We identified over 600 genes differentially expressed in organs of mice latently infected with MHV68 and found distinct sets of genes linked to different pathways were altered in spleen compared to liver. Several of the most differentially expressed latency-specific genes (e.g. IFNγ, Cxcl9, Ccl5) are associated with known latency-specific phenotypes. RNA was extracted from livers, spleens and brains of 7-9 week old male C57Bl/6 mice infected with gammaherpesvirus 68 (MHV68), a virus defective in establishment of latency (ORF73.stop) or mockulum. RNA from 3-4 mice per treatment was pooled and analyzed by M430 2.0 Affymetrix Gene Chip. Three biologic replicates were analyzed for all conditions, except mock livers, for which four biologic replicates were analyzed.
2013-10-18 | E-GEOD-51365 | biostudies-arrayexpress
Project description:MHV68 ORF50stop Vaccine Gene Expression
| PRJNA945888 | ENA
Project description:Previous studies identified a role for latent herpesvirus infection in cross-protection to infection and exacerbation of chronic inflammatory diseases. Here, we compared the gene expression signature from livers, spleens and brains of mice infected with wild-type gammaherpesvirus 68 (MHV68), a mutant virus defective in the establishment of latency (ORF73.stop) or mockulum. We identified over 600 genes differentially expressed in organs of mice latently infected with MHV68 and found distinct sets of genes linked to different pathways were altered in spleen compared to liver. Several of the most differentially expressed latency-specific genes (e.g. IFNγ, Cxcl9, Ccl5) are associated with known latency-specific phenotypes.
2013-10-18 | GSE51365 | GEO
Project description:Gammaherpesviruses (GHV) are DNA tumor viruses that establish lifelong latent infections in lymphocytes. For viruses such as Epstein-Barr virus (EBV) and murine gammaherpesvirus 68 (MHV68), this is accomplished through a viral gene-expression program that promotes cellular proliferation and differentiation, especially of germinal center (GC) B cells. Intrinsic host mechanisms to control virus-driven cellular expansion are incompletely defined. Using a small-animal model of GHV pathogenesis, we identify the B cell-specific latency gene M2, an MHV68 mediator of GC B cell differentiation, as a viral gene product that is sufficient to induce p53 in a manner that is dependent on Src kinase activity. To understand the function of M2 in primary B cells, we performed retroviral transduction of M2 or M2.Stop in wild-type or p53-deficient B cells. Our results reveal p53 and cellular proliferation pathways enriched in M2-expressing B cells.
2024-12-19 | GSE225579 | GEO
Project description:Vero cells were infected with Zika virus in three biological replicates and sampled at three post-infection timepoints (12 hrs, 24 hrs, 48 hrs). Biological replicate mock uninfected cells were also done for each timepoint. We used TMT6 labeled quantitation at each timepoint to examine proteome changes in response to infection.
2020-03-05 | MSV000085057 | MassIVE
Project description:mRNA-seq of AID-expressing cells from mice infected with WT or M2.Stop 73.Bla MHV68
| PRJNA1201157 | ENA
Project description:Objective: Multiple sclerosis (MS) is a chronic, autoimmune disease of the central nervous system. Prior infection with Epstein-Barr virus (EBV), a gammaherpesvirus, is deemed a necessary yet insufficient factor in the development of MS. The objective of this study was to determine whether the EBV-like virus, murid gammaherpesvirus 68, is sufficient to induce inflammatory demyelinating disease in a transgenic TCR mouse strain susceptible to CNS autoimmunity. Methods: B10.PL mice that express the myelin basic protein-specific transgenic T cell receptor (TCRMBP) were intranasally inoculated with murid gammaherpesvirus 68 virus (MHV68), PR8 influenza virus, or PBS. Mice were evaluated for the development of neurologic deficits. Flow cytometry and fluorescent microscopy were used to validate the infiltration of immune cells in the brain and spinal cord of TCRMBP mice. Single cell RNA sequencing of splenic B cells was performed to determine transcriptional changes that resulted from MHV68 infection. Results: MHV68-infected mice developed neurological deficits at a significantly higher frequency (70.8%) than the influenza (7.7%) or mock-infected mice (13.3%). MHV68 infected mice exhibited signs including optic neuritis and ataxia, which are infrequently observed in EAE mice, but common in MS patients. MHV68-infected mice exhibited increased focal immune cell infiltration. Single cell RNA sequencing identified the emergence of a novel, MHV68 infection-associated population of memory-like B cells that highly express genes associated with antigen presentation and costimulation. Conclusion: Infecting myelin basic protein specific TCR transgenic mice with the EBV analogue, MHV68, generates encephalitogenic disease without myelin immunization. MHV68 drives a distinct transcriptional program in B cells capable of enhanced antigen presentation and costimulation to drive an autoreactive T cell response.
2024-04-02 | GSE261605 | GEO
Project description:We performed RNA-seq to examine the differences in GC B cells that were either infected with MHV68 or uninfected and between B cells that expressed IgL or IgK B cell receptor light chains.
2020-03-02 | GSE140056 | GEO
Project description:We applied a tRNA-specific sequencing pipeline to analyze tRNA expression during infection of MC57G fibroblasts with the gammaherpesvirus MHV68. We find that expression of 14% of tRNA genes is significantly upregulated during infection. By mapping reads to either premature tRNA (pre-tRNA) or mature tRNA sequences, we find that increased expression of tRNA genes is manifested at the level of the pre-tRNA only, indicating a homeostatic mechanism to maintain the size and composition of mature tRNA pools.
2019-12-20 | GSE142393 | GEO